The clinical assessment of apraxia
As a definition of exclusion, this has led to the confusion that many of the movement disorders are described as forms of disassociation, although many of them fail to capture the essence of disassociation: motor cognitive impairment.
Apraxia reflects impaired storage and transformation of motor performance in the brain, either by reducing the semantic knowledge used by gestures and tools, either by being unable to accurately translate the neural representation of higher-level targets into low-level patterns of muscle activation and inhibition.
ApraxiaOur\'s current clinical approach to apraxia is similar to the approach proposed by Liepman in the early 20 th century.
He recognized that left hemisphere lesions could lead to bilateral upper limb loss and proposed a model of motion control in which the left parietal lobe stores the \"space-time form picture\" of movement \".
To perform a motion, it is necessary to retrieve and activate its picture, and then associate it with the associated motion engram in the frontal lobe region through a cortical projection.
From here, the information is transmitted to the primary motor cortex, which is then fed to the spinal bundle of the cortex.
In order for the right upper limb to move the information in the left hemisphere, however, for the left upper limb to move the information from the left parietal lobe, it must first be sent to the right frontal lobe and frontal region through a corpus. oas_tag. loadAd(\"Middle1\");
Liepman used this scheme to describe three forms of apraxia.
He described the conceptual loss as an interruption of the space-time picture, in which the concept of motion itself is lost or degraded.
In the conscious movement apraxia, the idea of motion is complete, but it cannot be accurately mapped to the motor engram of the frontal lobe.
The destruction of these engram caused \"melokinetichi\" apraxia (Now it\'s called limb.
Power apraxia, see below)
Interference controlled by fine motor.
Therefore, the interference of conceptual movement system and conscious movement and body movement is secondary
The power loss is caused by the interference of the action production system.
Conceptual concepts, concepts of movement and intention are degraded and patients may not understand the proper use of the tool.
For example, 2 patients presented with scissors can name the object correctly, but may not be able to describe their use.
When the examiner proves their use, the patient may not be able to distinguish between the action performed poorly and the action performed correctly.
When they hand the items themselves, it may be difficult for them to cut a piece of paper with them.
This indicates the loss of conceptual or semantic knowledge of what scissors are and their use.
Therefore, patients with conceptual loss of association cannot use mime tools to direct.
They may also lose the basic semantic knowledge behind simple gestures and may not be able to show how to wave goodbye or how to wave.
Because the action-making system remains complete, the examiner should be able to perform these tasks when giving these patients a visual presentation.
However, in practice, any damage or degradation process that affects the conceptual motor system also often affects the action-generating system, so they do not necessarily show this separation.
Distinguishing between ideological and ideological motor loss is not helpful for lesion localization.
Although the lower parietal lobe is more relevant to the conceptual motor system, there is no convincing correlation between the damage here and the conceptual loss;
Similarly, although the top lobe is more related to the action generation system, the three injuries here are not related to the occurrence of loss of consciousness movement.
1 patients with ideal loss of association are often very disabled and struggle greatly when trying to carry out basic activities of daily life.
It usually develops in people with Alzheimer\'s disease (
People who also often have memory and language barriers)
Stroke patients in the left hemisphere (
People who often have pronunciation disorders and half-body failure).
What is described above is equivalent to the interruption of the concept of motion, so some authors describe this type of deficit as \"conceptual failure \";
It is confusing that they use \"conceptual apraxia\" instead, referring to the inability to link complex task sequences when pursuing the overall goal, such as bubble one
Others, however, believe that this difficulty is a manifestation of the production system of action and classify this defect as a form of movement of consciousness.
As discussed below, practical neurologists can reasonably avoid these problems by being completely away from the term!
The loss of mental movement is a disorder in the movement production system.
Affected patients show errors in scaling, time and direction of movement, and may also omit or repeat individual elements of the overall action being evaluated.
It is difficult for them to produce meaningful, arbitrary hand poses, and they tend to perform poorly when asked for mime movements.
A common mistake is \"body-part-as-
\"Object error\", when asked for a particular action of a mime, the patient replaces the relevant tool with the body part.
For example, when asked to show how to comb your hair, comb your hair with your fingers and rub your teeth with your fingers when asked to show how to use your toothbrush.
These errors may also occur in healthy people, and they should only be considered pathological after they are emphasized to patients.
Despite these difficulties, the target of the action can usually be identified, and a typical feature is that if the patient is given an object that has just been asked for a mime, the patient\'s performance will be significantly improved;
5 because the overall goal of the action has a complete representation, visual and tactile feedback with association with the natural use of the object can improve the selection of appropriate limb poses and finger configurations.
Therefore, patients with mental motor loss may be less disabled than patients with mental motor loss.
Although it was previously thought that the disease was mainly identifiable in clinical examinations and had little effect on the day to dayto-
The function of the day is not necessarily like this;
It usually leads to serious dysfunction. 6Limb-
In addition to introducing the two terms of concept and concept movement apraxia, Liepman also describes \"melokinetichi\" apraxia, where the overall \"plot of complex movements
Later changed its name to body
Dynamic loss of contact, which is characterized by loss of contact
Coordination between fine, personalized finger movements required to perform skilled tasks.
This is due to the interruption of the final stage of the motor processing in the frontal lobe region before the information is transmitted to the lateral primary motor cortex.
Thus, damage affecting a forehead lobe or its connection can result in limb-
The power loss of the lateral upper limb.
This form of disassociation is largely ignored because it is often considered a purely dexterity problem rather than a real disassociation problem, although it is a disorder of motor control, it is firmly above the pyramid and the outer system of the cone.
Another possible reason for its relatively low profile is that any damage affecting the motor cortex of the frontal lobe may also damage the integrity of the spinal cord bundles of the cortex, so muscle weakness usually masks any higher levels of motor control disorders
As a result, the term is not widely used, but with many patients with cortical nasal syndrome having limbs, there is renewed interest in the field.
Lack of momentum for economic growth.
8 It often occurs early in the course of the disease, and neurologists should suspect that if the patient tries to produce any form of rhythm confrontation between the index finger and the thumb when testing motor retardation.
Sometimes, it is easier to prove this by asking the patient to quickly compare the thumb to the index finger, middle finger, ring finger and small finger in turn.
Because patients with limbs
Sports loss can not easily produce personalized finger movements, just like patients with mental loss, it is also very difficult to imitate meaningless gestures. 9 While limb-
Exercise loss of summer is often a prominent feature of cortical nasal syndrome, which often coexist with conscious movement and ideological loss of summer.
8 Language loss and facial loss need to transform the neural representation of grammatical sentences into an accurate pattern of facial muscle activity;
The interruption of this process is called the summer of speech.
Patients with speech loss have slow, deliberate and laborious speech.
They may make mistakes in the shape, order, and production time of a single syllable, and may display \"pronunciation fumbling\", correcting themselves repeatedly when trying to find the right word or sound.
The rhythm of the voice is also greatly affected by the loss of natural rhythm, intonation and overall melody.
Although no single brain region is fully involved, the loss of speech is closely related to the lesions of the left lower frontal return and the left anterior Island.
11 It usually occurs in patients with stroke or progressive non-stroke
Therefore, there are often some language barriers to coexistence.
Distinguishing speech loss from speech disorder may be a challenge (
And beyond the scope of this article)
Although the mouth surface is determined (see below)
It is generally believed that voice loss is an important reason for voice interference.
It may also be difficult to distinguish between speech and speech, but it is difficult to pronounce words, but when one syllable is repeated
For example, \"pa, pa . . . . . . \")
Patients with dysarism often make mistakes in time and pronunciation, and patients with lost speech are usually not difficult.
However, when asked to string multiple syllables together, they usually struggle very hard (eg, ‘pa-ta-ka, pa-ta-ka, …’).
10 Another useful clue is that patients with dysarism may pronounce errors in a consistent manner, in terms of pronunciation errors in patients with lost speech between one use of a specific word and the next use
The mouth surface refers to the inability to conduct non-proficiencyspeech-
Related movements involving tongue and facial muscles;
It is associated with damage to the premotor cortex of the abdomen.
Its assessment includes asking patients to cough or click on their tongue and show how they can drink or blow matches through a straw.
While it can happen in isolation, it almost always coexists with speech and/or language barriers.
Before starting to assess whether there is a loss of use, clinicians should conduct a careful neurological examination of the patient to ensure that the patient\'s motor symptoms cannot be explained by muscle weakness, spasm, slow exercise, ataxia, or loss of feeling.
The following is a protocol to check for loss of association in which patients are required to use a mime tool to produce meaningful and meaningless gestures and perform a movement sorting task (see table 1).
Looking at this table: Looking at the inline View pop-up table 1 the pattern for checking the praxisThis basic check sequence has evolved as specific damage patterns help to classify apraxia as one of the above three categories although in practice, most patients with apraxia are deficient in concept and production systems.
Given that the definitions of these terms are also not generally accepted (
That is to say, is the conceptual loss of contact \"conceptual\" loss of contact, or can\'t the task of movement be sorted? )
, There is a strong reason to omit them from the description of any apraxia patient.
Thus, while one can carefully try to find out any anatomical and pathological significance that may be separated as observed in assessing the different behaviors described above, it is best to simply treat these tests as providing a way to test the action production system in a variety of ways.
Therefore, when it comes to documenting a person\'s findings, it is sufficient to describe only the affected body parts and the damaged movements.
Despite this simplified approach, there is still some practical value in understanding a patient with an obviously asymmetrical hand clumsiness (
Can not imitate any posture)
There are probably limbs. Power loss;
This should make neurologists aware of the possibility of cortical nasal syndrome.
A sensible starting point in the examination scheme is to observe the use of patient mime tools by issuing a command such as \"pretend you have a hammer in your hand and show me how you can hammer with a hammer \".
Other useful dummies include having patients show how to use scissors, bottle openers, or brush their teeth.
Mistakes should only be considered morbid if they still exist after they have been corrected.
If the action is defective at the time of the order, then the examiner can consider demonstrating the correct pantomime and then ask the patient to imitate.
The idea is that a patient with conceptual loss of association may not be able to show this action because they have lost the semantic memory associated with this tool, however, if they can see how it should be used, then they can still access the basically complete action production system and then produce a good imitation.
However, for the above reasons, there is very little such neat separation in clinical practice.
Patients should then be asked to show a few meaningful gestures, including waving goodbye, motioning \"come here\", salutation, and a ride.
If buccofacial apraxia is tested, then clinicians may ask patients to cough, lick their lips, and show how they can drink or blow matches through a straw.
Because conceptual and motion-generating systems are often confined to the left hemisphere, most patients with defects in using pantomming tools and producing meaningful gestures have left hemisphere lesions and have bilateral loss
Then the examiner may ask the patient to imitate some arbitrary hand position (
Figure 1 gives an example.
Should show the patient gestures in the mirror
Just like the fashion when assessing the patient\'s left hand, the Examiner demonstrates it with his right hand.
The difficulty of this task may be physical performance.
Since this may be a secondary cause of unilateral frontal lobe injury, this should be evaluated in both hands.
Download figureOpen in the new tabDownload powerpoint figure 1 to show an example of any hand posture when evaluating apraxia patients.
Adapted from Goldenberg.
The evaluation should be done by sorting tasks such as the three-step command.
The examiner should alternately tap a surface with the side of the fist, the edge of the hand and the palm of the hand (figure 2)
Done several times before asking the patient to do the same.
While this task clearly tests the integrity of the action production system, impaired working memory or execution function can also result in poor performance.
Download the new tabDownload figureOpen powerpointFigure2 three-hand position by lurea three
Step sort task.
As mentioned above, other forms of apraxia, the traditional definition of apraxia is that it is impossible to perform the task of movement, and the inability of movement, loss of feeling or lack of understanding, cannot be fully explained.
In general, however, apraxia is considered to be unable to perform skilled sport tasks, followed by interference from the motor function of the superior.
As a result, several diseases that were initially marked as missing form are no longer generally considered to be the case.
Constructive apraxia is a method that cannot accurately copy drawings or 3D structures.
The underlying problem, however, is visual space processing, not higher-level motor control, so this should not be seen as a real loss of use.
Similarly, patients wearing clothes lack the visual spatial capabilities required to properly locate clothing items.
Patients with open eyelids and lost contact are temporarily unable to open their eyelids.
The exact mechanism is still uncertain, but this may be a nuclear upper control disorder of eyelid elevation, requiring simultaneous activation of the lifting muscle and inhibition of the eye wheel array muscle.
While this may indeed be a more advanced disorder of motion control, the act of opening your eyes is basically automatic and unskilled at all;
So most authorities will not consider this to be a real apraxia.
Because it seems to be caused by an abnormal co-
The contraction of the muscles of the activator and the activator may be best considered as a form of tension disorder, in fact, many patients who have lost their lids also have eyelid spasm.
Eye movement loss refers to the inability to actively scan the visual target.
Its foundation is that the function of the posterior parietal region is impaired and the visual attention cannot be directed to the appropriate part of the outside world.
Although this ultimately shows a motor shortage, it is not a secondary motor control interference and therefore is not a real loss of use.
Gait loss is defined as \"loss of the ability to properly use the lower limbs during walking, which cannot be explained by obvious sensory disorders or motor defects \".
It is characterized by slow speed, short number of steps, hesitation, wide base, and freezing of gait.
This gait is usually caused by bilateral brain disease and often occurs in normal stress water accumulation, Alzheimer\'s disease and diffuse cerebral vascular disease.
As a result, many of the affected patients had overall cognitive impairment accompanied by signs of the pyramid and the extragramid system, although they generally did not have simultaneous upper limb loss.
Therefore, its classification is apraxia (
A disorder of pure superior motor control)
Was challenged with high terminology
Horizontal gait disorders have been proposed. 18Case 1A 64-year-
A 6-year-old was referred to neurology.
The progress of his left hand, the dominant hand, is \"weak\" for a month.
He described the increasing difficulty of many activities in daily life, including writing, using knives and forks and fastening buttons.
His wife reported that his thoughts and speeches had slowed down, but he still remembered the details of the day --to-
Activities and dialogue.
During the examination, there was mild lack of sleep, decreased swing of the left arm, but normal gait.
The eye movement he pursued was broken, but there was no nystagmus and the scan was normal.
There is no tremor in the limbs, no tension disorder, no muscle weakness.
Mild stiffness of the right upper limb and severe stiffness of the left upper limb.
The right hand has a slight slow movement, but he cannot perform an orderly repetitive movement with his left hand.
He could not imitate the arbitrary hand position with his left hand at all, but his right hand was only slightly difficult.
When asked to brush his teeth in pantomime, he rubbed the sides of his teethand-
Back and forth with one side of the left index finger.
He can easily show the salute, but he has a hard time making a beckoning action with his left index finger, and often goes wrong when trying the three actions of Loriastep command.
This person is suffering from Parkinson\'s disease and has a serious loss of access to the left upper limb.
This is mainly manifested in the lack of flexibility and the discovery of prominent limbs by neurological examinationPowered Flying Man
Brain MR scans showed mild systemic atrophy and more focal atrophy in the right parietal lobe (figure 3).
His symptoms did not respond to left dopamine and we were diagnosed with corticobasal syndrome.
Download the new tabDownload figureOpen powerpointFigure3 MR to scan the brain (
Corona slice recovered by fluid attenuation reversal (FLAIR)sequences)
In a patient with cortical nasal syndrome, extensive atrophy was shown, and the area of the right parietal lobe was more severely affected. Case 2A 74-year-
Old women have a long history of cognitive impairment.
She has been trying to remember the details of the day for two years --to-
Day event and recently developed word-
Over the past few months, she has become more dependent on her husband in terms of basic activities in her daily life, and now she can\'t drink tea, using knives and forks or any household appliances.
Routine neurological examination is difficult due to the inability to check together
Operate using basic motion instructions, but this is normal in addition to the broken chasing eye movements and positive grip reflections.
When she was asked to comb her hair with a pantomime, she opened her palm and waved it on her face;
When asked for the mime to clean her teeth, she slowly moved her palm to her lips as she closed her mouth.
She could wave goodbye, but not pay tribute to the order.
It is difficult for her to position some of her figures to match the examiner\'s casual hand posture.
The woman suffered from severe loss of use in the context of progressive amnesia and language disorder and was diagnosed with Alzheimer\'s disease.
Her performance in pantoming\'s simple activities was very poor, indicating that she had no conceptual understanding of the required actions and that she had a conceptual apraxia.
Her flaws may represent the downstream effects of a flawed conceptual motor system, but it is likely that she also has a certain degree of loss of consciousness movement.
If we prove that she cannot use a toothbrush or comb when presenting these things, the label of the ideal apraxia would be safer, but such a distinction may not affect her diagnosis or treatment.
The key issue is that in the higher level motor control process, skilled motor tasks cannot be performed due to interference.
In conceptual cognition, the concept of movement and intention is degraded and patients may not be able to understand the appropriate use of the tool.
In conscious motor loss, patients cannot convert a neural representation of an idea or goal into an exact pattern of motor activity, so errors can occur in scaling, time and direction of movement. In limb-
Power loss, fine personalized hand motor collapse, usually from damage to the lateral prefrontal cortex or associated subcortex pathway;
This is often very prominent in patients with cortical nasal syndrome.
The loss of these forms is clinically difficult to solve;
A practical solution is to ask the action production system by asking the patient to perform a variety of motion tasks.
Dr. Xie, author of acknoughtmentsthe, Ana thans Ampatuan manuscript has put forward useful opinions.
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